A number of studies in which anti-oxidant status has been raised by dietary supplementation indicate that improvement of anti-oxidant status is associated with an increase in cellular aspects of immune function. Vitamin E exerts modulatory effects on both inflammatory and immune components of immune function. In general, vitamin E deficiency and low tissue vitamin E content enhance components of the inflammatory response and suppress components of the immune response. Dietary vitamin E supplementation brings about the opposite effect. Studies in animals have demonstrated that vitamin E deficiency impairs cellular and humoral immunity and is associated with an increased incidence of disease. Supplementation of the diet with vitamin E, at levels that are several fold greater than requirements, increases resistance to a number of pathogens. Resistance of chickens and turkeys to Escherichia coli and of mice to pneumococci, was enhanced by vitamin E supplementation. A similar phenomenon may also occur in humans, since epidemiological evidence shows lower incidence of infectious disease in subjects with high plasma «-tocopherol concentrations. Rats consuming diets that were deficient in vitamin E, and given injections of endotoxin, showed a greater degree of anorexia and greater concentrations of plasma «-1-acid glycoprotein and IL6, than animals consuming adequate amounts of the vitamin. In smokers, a low intake of vitamin E was associated with an increased intensity of the inflammatory response to cigarette smoke. Plasma concentrations of «-1-acid glycoprotein was 50% higher in subjects in the lowest tertile of intake compared with the values for subjects in the highest tertile (57). Large doses of «-tocopherol 50 mg/kg given i.p. significantly decreased the number of neutrophils in airspaces of rats given endotoxin aerosols; however, there appeared to be no change in NFkB or AP1 activation (58).
Supplementation of the diet of healthy subjects, and smokers with 600 IU/ day «-tocopherol, for 4 weeks, suppressed the ability of PBMCs to produce TNF-« (59). Intense exercise of healthy young and elderly subjects results in the appearance of a mild inflammatory response characterized by raised blood IL1, IL6, and acute phase protein concentrations. A twice daily supplement of 400 IU of «-tocopherol inhibited the response.
A dose of 600IU/day «-tocopherol given to healthy elderly subjects, for 235 days, increased delayed type hypersensitivity and raised antibody titers to hepatitis B (60). When elderly subjects were supplemented with 800 IU of «-tocopherol for 30 days, there was a 50% increase in the delayed type hypersensitivity response, a 65% increase in IL-2 production, and a decrease in oxidative stress as indicated by a major decrease in plasma thiobarbituric acid substances (TBARS). An enteral feed, enriched with vitamin E, vitamin C, and taurine, given to intensive care patients decreased total lymphocyte and neutrophil content in bronchio-alveolar lavage fluid (decreased inflammation) and resulted in a reduction in organ failure rate, reduced requirement for artificial ventilation, and a reduction of 5 days in the requirement for intensive care (61). These results highlight that reduced inflammation and improved immune function are interrelated.
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